The effect of chronic cerebral hypoperfusion on the pathology of Alzheimer's disease: A positron emission tomography study in rats

• Published in: Scientific reports 2019-10, Vol.9 (1), p.14102-9, Article 14102
• Main Authors: Park, Jae-Hyung, Hong, Jeong-Ho, Lee, Sang-Woo, Ji, Hyun Dong, Jung, Jung-Ah, Yoon, Kyung-Wha, Lee, Jung-In, Won, Kyoung Sook, Song, Bong-Il, Kim, Hae Won
• Format: Article
• Language: English
• Subjects: 59; 59/78; 631/378/2607; 631/378/2649/2150; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Alzheimer's disease; Amygdala; Amyloid; Amyloid beta-Peptides - metabolism; Animals; Apoptosis; Brain - metabolism; Brain - pathology; Brain Ischemia - metabolism; Brain Ischemia - pathology; Carotid artery; Cerebral infarction; Cerebrovascular Circulation - physiology; Cerebrovascular diseases; Cerebrovascular Disorders - metabolism; Cerebrovascular Disorders - pathology; Cognition Disorders - metabolism; Cognition Disorders - pathology; Cognitive ability; Cortex (entorhinal); Cortex (frontal); Disease Models, Animal; Emissions; Glucose; Glucose metabolism; Hippocampus; Humanities and Social Sciences; Male; Metabolism; multidisciplinary; Neurodegenerative diseases; Neurons - metabolism; Neurons - pathology; Pathology; Positron emission tomography; Positron-Emission Tomography - methods; Rats; Rats, Wistar; Risk factors; Rodents; Science; Science (multidisciplinary); Tau protein; Temporal lobe; Tomography, X-Ray Computed - methods; Western blotting
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-019-50681-4

Cerebrovascular disease is a potential risk factor for Alzheimer's disease (AD). Although acute cerebral hypoperfusion causes neuronal necrosis and infarction, chronic cerebral hypoperfusion induces apoptosis in neurons, but its effects on the cognitive impairment are not clear. The purpose of this study was to evaluate the effects of chronic cerebral hypoperfusion on AD pathology and cerebral glucose metabolism. A model of chronic cerebral hypoperfusion was established by ligating the common carotid arteries bilaterally in adult male rats (CAL group). Sham-operated rats underwent the same procedures without artery ligation (control group). At 12 weeks after ligation, expression levels of amyloid-β (Aβ) and hyperphosphorylated tau (p-tau), as well as the regional cerebral glucose metabolism, were evaluated using Western blots and positron emission tomography with fluorine-18 fluorodeoxyglucose, respectively. The expression levels of Aβ in the frontal cortex and hippocampus and of p-tau in the temporal cortex were significantly higher in the CAL group than those in the control group. The cerebral glucose metabolism of the amygdala, entorhinal cortex, and hippocampus was significantly decreased in the CAL group compared to that in the control. These results suggest that chronic cerebral hypoperfusion can induce AD pathology and may play a significant role in AD development.